Vanderhyden B C, Macdonald E A
a Ottawa Regional Cancer Centre, and Departments of Medicine, Cellular and Molecular Medicine, and Obstetrics&Gynecology, University of Ottawa, Ottawa, Ontario, Canada K1H 8L6.
Biol Reprod. 1998 Dec;59(6):1296-301. doi: 10.1095/biolreprod59.6.1296.
Mouse oocytes secrete a factor(s) that inhibits progesterone and enhances estradiol production by granulosa cells. This study determined the ability of mouse oocytes to secrete this steroid-regulating factor during oocyte growth and the ability of granulosa cells to respond to the factor during follicular development. Oocyte-granulosa cell complexes from preantral and antral follicles were oocytectomized (OOX; oocytes microsurgically removed) and cultured for up to 48 h with FSH (150 ng/ml) and testosterone (500 nM). At all stages of development examined, OOX complexes produced more progesterone than did intact complexes, from 1.45-fold for early growing follicles to 23-fold for complexes from antral follicles. Significant estradiol production was restricted to intact complexes from late antral follicles. Progesterone accumulation by OOX complexes cocultured with oocytes was inhibited by all stages of oocytes examined, with maximal inhibition by fully grown oocytes. Ovulated complexes produced large quantities of progesterone, even though oocytes secreted progesterone-inhibitory factor, because of a desensitization of cumulus cells to the factor during their terminal differentiation. Even in the presence of abundant pregnenolone, OOX complexes showed reduced ability to produce and/or accumulate progesterone in the presence of oocytes, suggesting that the oocyte-secreted factor, either directly or indirectly, regulates the activity of 3beta-hydroxysteroid dehydrogenase and/or progesterone metabolism. These results demonstrate that oocytes secrete a factor with steroid-regulating activity in increasing amounts and/or potency during follicular development, but responsiveness of cumulus cells to this factor declines during luteinization.
小鼠卵母细胞分泌一种因子，该因子可抑制孕酮，并增强颗粒细胞产生雌二醇的能力。本研究确定了小鼠卵母细胞在卵母细胞生长过程中分泌这种类固醇调节因子的能力，以及颗粒细胞在卵泡发育过程中对该因子的反应能力。对来自窦前卵泡和窦卵泡的卵母细胞-颗粒细胞复合体进行卵母细胞切除（OOX；通过显微手术去除卵母细胞），并与促卵泡激素（FSH，150 ng/ml）和睾酮（500 nM）一起培养长达48小时。在所有检测的发育阶段，OOX复合体产生的孕酮都比完整复合体多，从早期生长卵泡的1.45倍到窦卵泡复合体的23倍。显著的雌二醇产生仅限于来自晚期窦卵泡的完整复合体。与卵母细胞共培养的OOX复合体中孕酮的积累受到所有检测阶段卵母细胞的抑制，完全成熟的卵母细胞抑制作用最大。排卵复合体产生大量孕酮，尽管卵母细胞分泌孕酮抑制因子，但由于卵丘细胞在终末分化过程中对该因子脱敏。即使存在大量孕烯醇酮，在有卵母细胞存在的情况下，OOX复合体产生和/或积累孕酮的能力也会降低，这表明卵母细胞分泌的因子直接或间接调节3β-羟基类固醇脱氢酶的活性和/或孕酮代谢。这些结果表明，在卵泡发育过程中，卵母细胞分泌的具有类固醇调节活性的因子数量和/或效力不断增加，但卵丘细胞对该因子的反应性在黄体化过程中下降。
